MiR-373在多種腫瘤中均出現異常表達，扮演著癌基因或者抑癌基因的角色，影響腫瘤細胞的增殖、侵襲和轉移過程。有研究報道miR-373在乳腺癌中表達上調，通過下調CD44的表達而促進腫瘤細胞的侵襲轉移能力。在人纖維肉瘤HT1080細胞中，過表達的miR-373可直接通過靶向結合雷帕霉素靶蛋白(mechanistic target of rapamycin, mTOR)和去乙酰化酶1(sirtuin 1, SIRT1)mRNA的 3 UTR而使mTOR和SIRT1的表達下調，進一步導致Ras/Raf/MEK/Erk信號通路和轉錄因子(nuclear factor kappa B, NF-κB)的激活，從而提高MMP-9的表達水平，增強腫瘤細胞的生長和遷移能力。Zhang等研究發現miR-373在胃癌中高表達，通過下調靶基因腫瘤壞死因子α誘導蛋白1(tumor necrosis factor, alpha-induced protein 1, TNFAIP1)的表達而促進胃癌細胞的增殖。然而，miR-373與肺癌的研究甚少，兩者的關系尚未十分明確。

miR-373 is abnormally expressed in many types of tumors. It may function as an oncogene or a tumor suppressor gene and influence the proliferation, invasion, and metastasis of tumor cells. Previous studies have reported that miR-373 is upregulated in breast cancer and that it promotes tumor cell invasion and metastasis by downregulating CD44 expression. In HT1080 human fibrosarcoma cells, overexpressed miR-373 may directly target the 3′ UTRs of the mRNAs of mechanistic target of rapamycin (mTOR) and sirtuin 1 (SIRT1). Consequently, mTOR and SIRT1 are downregulated, thereby activating the Ras/Raf/MEK/Erk signaling pathway and the transcription factor nuclear factor kappa B (NF-κB). This results in an increase in matrix metallopeptidase 9 (MMP-9) expression and an enhancement in the growth and migratory abilities of tumor cells. Zhang et al. have shown that miR?373 is upregulated in gastric cancer and that it promotes the proliferation of gastric cancer cells by downregulating tumor necrosis factor, alpha-induced protein 1 (TNFAIP1). However, the relationship between miR 373 and lung cancer remains unclear owing to a lack of relevant research.